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Predicting Gene Ontology Biological Process from Temporal Gene Expression Patterns Astrid Lægreid,1,4 Torgeir R
Methods Predicting Gene Ontology Biological Process From Temporal Gene Expression Patterns Astrid Lægreid,1,4 Torgeir R. Hvidsten,2 Herman Midelfart,2 Jan Komorowski,2,3,4 and Arne K. Sandvik1 1Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, N-7489 Trondheim, Norway; 2Department of Information and Computer Science, Norwegian University of Science and Technology, N-7491 Trondheim, Norway; 3The Linnaeus Centre for Bioinformatics, Uppsala University, SE-751 24 Uppsala, Sweden The aim of the present study was to generate hypotheses on the involvement of uncharacterized genes in biological processes. To this end,supervised learning was used to analyz e microarray-derived time-series gene expression data. Our method was objectively evaluated on known genes using cross-validation and provided high-precision Gene Ontology biological process classifications for 211 of the 213 uncharacterized genes in the data set used. In addition,new roles in biological process were hypothesi zed for known genes. Our method uses biological knowledge expressed by Gene Ontology and generates a rule model associating this knowledge with minimal characteristic features of temporal gene expression profiles. This model allows learning and classification of multiple biological process roles for each gene and can predict participation of genes in a biological process even though the genes of this class exhibit a wide variety of gene expression profiles including inverse coregulation. A considerable number of the hypothesized new roles for known genes were confirmed by literature search. In addition,many biological process roles hypothesi zed for uncharacterized genes were found to agree with assumptions based on homology information. -
Nº Ref Uniprot Proteína Péptidos Identificados Por MS/MS 1 P01024
Document downloaded from http://www.elsevier.es, day 26/09/2021. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. Nº Ref Uniprot Proteína Péptidos identificados 1 P01024 CO3_HUMAN Complement C3 OS=Homo sapiens GN=C3 PE=1 SV=2 por 162MS/MS 2 P02751 FINC_HUMAN Fibronectin OS=Homo sapiens GN=FN1 PE=1 SV=4 131 3 P01023 A2MG_HUMAN Alpha-2-macroglobulin OS=Homo sapiens GN=A2M PE=1 SV=3 128 4 P0C0L4 CO4A_HUMAN Complement C4-A OS=Homo sapiens GN=C4A PE=1 SV=1 95 5 P04275 VWF_HUMAN von Willebrand factor OS=Homo sapiens GN=VWF PE=1 SV=4 81 6 P02675 FIBB_HUMAN Fibrinogen beta chain OS=Homo sapiens GN=FGB PE=1 SV=2 78 7 P01031 CO5_HUMAN Complement C5 OS=Homo sapiens GN=C5 PE=1 SV=4 66 8 P02768 ALBU_HUMAN Serum albumin OS=Homo sapiens GN=ALB PE=1 SV=2 66 9 P00450 CERU_HUMAN Ceruloplasmin OS=Homo sapiens GN=CP PE=1 SV=1 64 10 P02671 FIBA_HUMAN Fibrinogen alpha chain OS=Homo sapiens GN=FGA PE=1 SV=2 58 11 P08603 CFAH_HUMAN Complement factor H OS=Homo sapiens GN=CFH PE=1 SV=4 56 12 P02787 TRFE_HUMAN Serotransferrin OS=Homo sapiens GN=TF PE=1 SV=3 54 13 P00747 PLMN_HUMAN Plasminogen OS=Homo sapiens GN=PLG PE=1 SV=2 48 14 P02679 FIBG_HUMAN Fibrinogen gamma chain OS=Homo sapiens GN=FGG PE=1 SV=3 47 15 P01871 IGHM_HUMAN Ig mu chain C region OS=Homo sapiens GN=IGHM PE=1 SV=3 41 16 P04003 C4BPA_HUMAN C4b-binding protein alpha chain OS=Homo sapiens GN=C4BPA PE=1 SV=2 37 17 Q9Y6R7 FCGBP_HUMAN IgGFc-binding protein OS=Homo sapiens GN=FCGBP PE=1 SV=3 30 18 O43866 CD5L_HUMAN CD5 antigen-like OS=Homo -
Regulation of COX Assembly and Function by Twin CX9C Proteins—Implications for Human Disease
cells Review Regulation of COX Assembly and Function by Twin CX9C Proteins—Implications for Human Disease Stephanie Gladyck 1, Siddhesh Aras 1,2, Maik Hüttemann 1 and Lawrence I. Grossman 1,2,* 1 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA; [email protected] (S.G.); [email protected] (S.A.); [email protected] (M.H.) 2 Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services, Bethesda, Maryland and Detroit, MI 48201, USA * Correspondence: [email protected] Abstract: Oxidative phosphorylation is a tightly regulated process in mammals that takes place in and across the inner mitochondrial membrane and consists of the electron transport chain and ATP synthase. Complex IV, or cytochrome c oxidase (COX), is the terminal enzyme of the electron transport chain, responsible for accepting electrons from cytochrome c, pumping protons to contribute to the gradient utilized by ATP synthase to produce ATP, and reducing oxygen to water. As such, COX is tightly regulated through numerous mechanisms including protein–protein interactions. The twin CX9C family of proteins has recently been shown to be involved in COX regulation by assisting with complex assembly, biogenesis, and activity. The twin CX9C motif allows for the import of these proteins into the intermembrane space of the mitochondria using the redox import machinery of Mia40/CHCHD4. Studies have shown that knockdown of the proteins discussed in this review results in decreased or completely deficient aerobic respiration in experimental models ranging from yeast to human cells, as the proteins are conserved across species. -
Investigating Host Genes Involved In. HIY Control by a Novel Computational Method to Combine GWAS with Eqtl
Investigating Host Genes Involved in. HIY Control by a Novel Computational Method to Combine GWAS with eQTL by Yi Song THESIS Submitted In partial satisfaction of me teqoitements for the degree of MASTER OF SCIENCE In Biological and Medical Informatics In the GRADUATE DIVISION Copyright (2012) by Yi Song ii Acknowledgement First and foremost, I would like to thank my advisor Professor Hao Li, without whom this thesis would not have been possible. I am very grateful that Professor Li lead me into the field of human genomics and gave me the opportunity to pursue this interesting study in his laboratory. Besides the wealth of knowledge and invaluable insights that he offered in every meeting we had, Professor Li is one of the most approachable faculties I have met. I truly appreciate his patient guidance and his enthusiastic supervision throughout my master’s career. I am sincerely thankful to Professor Patricia Babbitt, the Associate Director of the Biomedical Informatics program at UCSF. Over my two years at UCSF, she has always been there to offer her help when I was faced with difficulties. I would also like to thank both Professor Babbitt and Professor Nevan Krogan for investing their valuable time in evaluating my work. I take immense pleasure in thanking my co-workers Dr. Xin He and Christopher Fuller. It has been a true enjoyment to discuss science with Dr. He, whose enthusiasm is a great inspiration to me. I also appreciate his careful editing of my thesis. Christopher Fuller, a PhD candidate in the Biomedical Informatics program, has provided great help for me on technical problems. -
High-Resolution Genomic Copy Number Profiling of Glioblastoma Multiforme by Single Nucleotide Polymorphism DNA Microarray
Published OnlineFirst May 12, 2009; DOI: 10.1158/1541-7786.MCR-08-0270 Published Online First on May 12, 2009 High-Resolution Genomic Copy Number Profiling of Glioblastoma Multiforme by Single Nucleotide Polymorphism DNA Microarray Dong Yin,1 Seishi Ogawa,3 Norihiko Kawamata,1 Patrizia Tunici,2 Gaetano Finocchiaro,4 Marica Eoli,4 Christian Ruckert,6 Thien Huynh,1 Gentao Liu,2 Motohiro Kato,3 Masashi Sanada,3 Anna Jauch,5 Martin Dugas,6 Keith L. Black,2 and H. Phillip Koeffler1 1Division of Hematology/Oncology and 2Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine, Los Angeles, California; 3Regeneration Medicine of Hematopoiesis, University of Tokyo, School of Medicine, Tokyo, Japan; 4National Neurological Institute “C Besta,” Milan, Italy; 5Institute of Human Genetics, University Hospital Heidelberg, Germany; and 6Department of Medical Informatics and Biomathematics, University of Munster, Munster, Germany Abstract growth factor receptor/platelet-derived growth factor receptor Glioblastoma multiforme (GBM) is an extremely malignant α. Deletion of chromosome 6q26-27 often occurred (16 of 55 brain tumor. To identify new genomic alterations in GBM, samples). The minimum common deleted region included genomic DNA of tumor tissue/explants from 55 individuals PARK2, PACRG, QKI,and PDE10A genes. Further reverse and 6 GBM cell lines were examined using single nucleotide transcription Q-PCR studies showed that PARK2 expression polymorphism DNA microarray (SNP-Chip). Further gene was decreased in another collection of GBMs at a expression analysis relied on an additional 56 GBM samples. frequency of 61% (34 of 56) of samples. The 1p36.23 region SNP-Chip results were validated using several techniques, was deleted in 35% (19 of 55) of samples. -
(ENO1), Identified As an Antigen to Monoclonal Antibody 12C7
Shu et al. Stem Cell Research & Therapy (2021) 12:119 https://doi.org/10.1186/s13287-021-02160-9 RESEARCH Open Access Alpha-enolase (ENO1), identified as an antigen to monoclonal antibody 12C7, promotes the self-renewal and malignant phenotype of lung cancer stem cells by AMPK/mTOR pathway Xiong Shu1†, Kai-Yue Cao2†, Hui-Qi Liu3, Long Yu4, Li-Xin Sun4, Zhi-Hua Yang4, Cheng-Ai Wu1* and Yu-Liang Ran4* Abstract Background: Tumor-associated antigens (TAAs) can be targeted in cancer therapy. We previously identified a monoclonal antibody (mAb) 12C7, which presented anti-tumor activity in lung cancer stem cells (LCSCs). Here, we aimed to identify the target antigen for 12C7 and confirm its role in LCSCs. Methods: Immunofluorescence was used for antigen localization. After targeted antigen purification by electrophoresis and immunoblot, the antigen was identified by LC-MALDI-TOF/TOF mass spectrometry, immunofluorescence, and immunoprecipitation. The overexpression or silence of ENO1 was induced by lentiviral transduction. Self-renewal, growth, and invasion of LCSCs were evaluated by sphere formation, colony formation, and invasion assay, respectively. High-throughput transcriptome sequencing (RNA-seq) and bioinformatics analysis were performed to analyze downstream targets and pathways of targeted antigen. Results: Targeted antigen showed a surface antigen expression pattern, and the 43–55 kDa protein band was identified as α-enolase (ENO1). Self-renewal, growth, and invasion abilities of LCSCs were remarkably inhibited by ENO1 downregulation, while enhanced by ENO1 upregulation. RNA-seq and bioinformatics analysis eventually screened 4 self-renewal-related and 6 invasion-related differentially expressed genes. GSEA analysis and qRT-PCR verified that ENO1 regulated self-renewal, invasion-related genes, and pathways. -
A Network Inference Approach to Understanding Musculoskeletal
A NETWORK INFERENCE APPROACH TO UNDERSTANDING MUSCULOSKELETAL DISORDERS by NIL TURAN A thesis submitted to The University of Birmingham for the degree of Doctor of Philosophy College of Life and Environmental Sciences School of Biosciences The University of Birmingham June 2013 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Musculoskeletal disorders are among the most important health problem affecting the quality of life and contributing to a high burden on healthcare systems worldwide. Understanding the molecular mechanisms underlying these disorders is crucial for the development of efficient treatments. In this thesis, musculoskeletal disorders including muscle wasting, bone loss and cartilage deformation have been studied using systems biology approaches. Muscle wasting occurring as a systemic effect in COPD patients has been investigated with an integrative network inference approach. This work has lead to a model describing the relationship between muscle molecular and physiological response to training and systemic inflammatory mediators. This model has shown for the first time that oxygen dependent changes in the expression of epigenetic modifiers and not chronic inflammation may be causally linked to muscle dysfunction. -
Chromosome Transfer Induced Aneuploidy Results in Complex Dysregulation of the Cellular Transcriptome in Immortalized and Cancer Cells
[CANCER RESEARCH 64, 6941–6949, October 1, 2004] Chromosome Transfer Induced Aneuploidy Results in Complex Dysregulation of the Cellular Transcriptome in Immortalized and Cancer Cells Madhvi B. Upender,1 Jens K. Habermann,1,4 Lisa M. McShane,3 Edward L. Korn,3 J. Carl Barrett,2 Michael J. Difilippantonio,1 and Thomas Ried1 1Genetics Branch and 2Laboratory for Biosystems and Cancer, Center for Cancer Research and 3Biometric Research Branch, National Cancer Institute/NIH, Bethesda, Maryland; and 4Department of Oncology and Pathology, Cancer Center Karolinska, Karolinska Institute, Stockholm, Sweden ABSTRACT tumor cells (4, 18–20). Additionally, in cell culture model systems in which cells are exposed to different carcinogens, chromosomal ane- Chromosomal aneuploidies are observed in essentially all sporadic uploidy is the earliest detectable genomic aberration (21, 22). carcinomas. These aneuploidies result in tumor-specific patterns of The conservation of these tumor and tumor-stage–specific patterns genomic imbalances that are acquired early during tumorigenesis, con- tinuously selected for and faithfully maintained in cancer cells. Although of chromosomal aneuploidies suggests that they play a fundamental the paradigm of translocation induced oncogene activation in hematologic biological role in tumorigenesis. It remains, however, unresolved how malignancies is firmly established, it is not known how genomic imbal- such genomic imbalances affect global gene expression patterns. One ances affect chromosome-specific gene expression patterns in particular could postulate that expression levels of all transcriptionally active and how chromosomal aneuploidy dysregulates the genetic equilibrium of genes on trisomic chromosomes would increase in accordance with cells in general. To model specific chromosomal aneuploidies in cancer the chromosome copy number. -
A High Resolution Atlas of Gene Expression in the Domestic Sheep (Ovis
bioRxiv preprint doi: https://doi.org/10.1101/132696; this version posted June 8, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Title: A high resolution atlas of gene expression in the domestic sheep (Ovis 2 aries) 3 4 Clark EL1ø*, Bush SJ1ø, McCulloch MEB1, Farquhar IL1‡, Young R1, Lefevre L1, Pridans C1, 5 Tsang HG1, Wu C2, Afrasiabi C2, Watson M1, Whitelaw CB1, Freeman TC1, Summers KM1, 6 Archibald AL1 and Hume DA1 7 8 1The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 9 Edinburgh, Easter Bush Campus, Edinburgh, Midlothian, EH25 9RG. 10 2Department of Integrative and Computational Biology, The Scripps Research Institute, 11 10550 North Torrey Pines Road, La Jolla, CA 92037. 12 ‡Current Address: Centre for Synthetic and Systems Biology, CH Waddington Building, Max 13 Borne Crescent, Kings Buildings, University of Edinburgh, EH9 3BF. 14 ø These two authors contributed equally to the work. 15 * Corresponding Author: [email protected] 16 17 18 19 20 21 22 23 24 25 1 bioRxiv preprint doi: https://doi.org/10.1101/132696; this version posted June 8, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 26 Abstract 27 28 Sheep are a key source of meat, milk and fibre for the global livestock sector, and an 29 important biomedical model. Global analysis of gene expression across multiple tissues has 30 aided genome annotation and supported functional annotation of mammalian genes. -
Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations Fall 2010 Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Renuka Nayak University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Computational Biology Commons, and the Genomics Commons Recommended Citation Nayak, Renuka, "Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress" (2010). Publicly Accessible Penn Dissertations. 1559. https://repository.upenn.edu/edissertations/1559 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1559 For more information, please contact [email protected]. Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Abstract Genes interact in networks to orchestrate cellular processes. Here, we used coexpression networks based on natural variation in gene expression to study the functions and interactions of human genes. We asked how these networks change in response to stress. First, we studied human coexpression networks at baseline. We constructed networks by identifying correlations in expression levels of 8.9 million gene pairs in immortalized B cells from 295 individuals comprising three independent samples. The resulting networks allowed us to infer interactions between biological processes. We used the network to predict the functions of poorly-characterized human genes, and provided some experimental support. Examining genes implicated in disease, we found that IFIH1, a diabetes susceptibility gene, interacts with YES1, which affects glucose transport. Genes predisposing to the same diseases are clustered non-randomly in the network, suggesting that the network may be used to identify candidate genes that influence disease susceptibility. -
Molecular Cytogenetic Analysis in the Study of Brain Tumors: Findings and Applications
Neurosurg Focus 19 (5):E1, 2005 Molecular cytogenetic analysis in the study of brain tumors: findings and applications JANE BAYANI, M.H.SC., AJAY PANDITA, D.V.M., PH.D., AND JEREMY A. SQUIRE, PH.D. Department of Applied Molecular Oncology, Ontario Cancer Institute, Princess Margaret Hospital, University Health Network; Arthur and Sonia Labatt Brain Tumor Research Centre, Hospital for Sick Children; and Departments of Laboratory Medicine and Pathobiology and Medical Biophysics, University of Toronto, Ontario, Canada Classic cytogenetics has evolved from black and white to technicolor images of chromosomes as a result of advances in fluorescence in situ hybridization (FISH) techniques, and is now called molecular cytogenetics. Improvements in the quality and diversity of probes suitable for FISH, coupled with advances in computerized image analysis, now permit the genome or tissue of interest to be analyzed in detail on a glass slide. It is evident that the growing list of options for cytogenetic analysis has improved the understanding of chromosomal changes in disease initiation, progression, and response to treatment. The contributions of classic and molecular cytogenetics to the study of brain tumors have pro- vided scientists and clinicians alike with new avenues for investigation. In this review the authors summarize the con- tributions of molecular cytogenetics to the study of brain tumors, encompassing the findings of classic cytogenetics, interphase- and metaphase-based FISH studies, spectral karyotyping, and metaphase- and array-based comparative genomic hybridization. In addition, this review also details the role of molecular cytogenetic techniques in other aspects of understanding the pathogenesis of brain tumors, including xenograft, cancer stem cell, and telomere length studies. -
The Essential and Downstream Common Proteins of Amyotrophic Lateral Sclerosis: a Protein-Protein Interaction Network Analysis
RESEARCH ARTICLE The essential and downstream common proteins of amyotrophic lateral sclerosis: A protein-protein interaction network analysis Yimin Mao1,2☯, Su-Wei Kuo2☯, Le Chen1, C. J. Heckman2,3,4, M. C. Jiang2* 1 Applied Science Institute, Jiangxi University of Science and Technology, Jiangxi, China, 2 Department of Physiology, Northwestern University, Chicago, Illinois, United States of America, 3 Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, Illinois, United States of America, 4 Department of Physical Therapy and Human Movement Sciences, Northwestern University, Chicago, a1111111111 Illinois, United States of America a1111111111 a1111111111 ☯ These authors contributed equally to this work. a1111111111 * [email protected] a1111111111 Abstract Amyotrophic Lateral Sclerosis (ALS) is a devastative neurodegenerative disease character- OPEN ACCESS ized by selective loss of motoneurons. While several breakthroughs have been made in Citation: Mao Y, Kuo S-W, Chen L, Heckman CJ, identifying ALS genetic defects, the detailed molecular mechanisms are still unclear. These Jiang MC (2017) The essential and downstream genetic defects involve in numerous biological processes, which converge to a common common proteins of amyotrophic lateral sclerosis: A protein-protein interaction network analysis. destiny: motoneuron degeneration. In addition, the common comorbid Frontotemporal PLoS ONE 12(3): e0172246. doi:10.1371/journal. Dementia (FTD) further complicates the investigation of ALS etiology. In this study, we pone.0172246 aimed to explore the protein-protein interaction network built on known ALS-causative Editor: Weidong Le, Institute of Health Science, genes to identify essential proteins and common downstream proteins between classical CHINA ALS and ALS+FTD (classical ALS + ALS/FTD) groups. The results suggest that classical Received: October 30, 2016 ALS and ALS+FTD share similar essential protein set (VCP, FUS, TDP-43 and hnRNPA1) Accepted: February 1, 2017 but have distinctive functional enrichment profiles.